Abstract
B10.S mice have been considered resistant to experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. However, sensitization with a myelin oligodendrocyte glycoprotein (MOG) peptide, MOG(92-106), induced clinical signs in 30% of mice and central nervous system (CNS) pathology in 93% of mice. Symptomatic mice had more demyelination, inflammation, perivascular cuffing and axonal damage in the CNS compared to asymptomatic mice, but no strong correlations between CNS pathology and clinical score were found. Interestingly, the ratio of B cells to T cells in cellular infiltrates correlated with clinical score. This suggests that the balance between B and T cells contributes to expression of clinical signs.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Antibody Formation
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Axons / immunology
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Axons / pathology
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B-Lymphocytes / immunology*
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Central Nervous System / immunology
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Central Nervous System / pathology
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Encephalomyelitis, Autoimmune, Experimental / pathology
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Immune Tolerance*
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Immunoglobulins / immunology
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Mice*
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Mice, Inbred Strains
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Multiple Sclerosis / immunology*
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Multiple Sclerosis / pathology
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Myelin Proteins
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Myelin-Associated Glycoprotein / genetics
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Myelin-Associated Glycoprotein / immunology*
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Myelin-Oligodendrocyte Glycoprotein
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T-Lymphocytes / immunology*
Substances
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Immunoglobulins
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Mog protein, mouse
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Myelin Proteins
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Myelin-Associated Glycoprotein
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Myelin-Oligodendrocyte Glycoprotein